The Role of Innate Immunity in Cardiovascular Diseases in Animals

Jeremy Novik^*
*Correspondence: Jeremy Novik, Department of Anesthesiology, University of Medicine and Pharmacy, 300041 Timisoara, Romania, Email:

Introduction

Cardiovascular Diseases (CVDs) are a leading cause of mortality and morbidity in animals, just as they are in humans. While the pathogenesis of CVDs in animals shares similarities with humans, there are distinct differences, including the role of innate immunity. Understanding how the innate immune system contributes to CVDs in animals is crucial for developing effective preventive and therapeutic strategies. This article explores the intricate interplay between innate immunity and cardiovascular diseases in animals [1].

The innate immune system serves as the first line of defense against pathogens and tissue injury in animals. Components of innate immunity include physical barriers, such as the skin and mucous membranes, as well as cellular and molecular mechanisms like phagocytes, natural killer cells and cytokines. Innate immunity plays a pivotal role in maintaining tissue homeostasis and responding to insults that contribute to cardiovascular diseases. Atherosclerosis, a hallmark of CVDs, is characterized by the accumulation of lipid-laden plaques in arterial walls. Innate immune cells, particularly macrophages and dendritic cells, contribute to the initiation and progression of atherosclerosis through inflammatory processes. Lipid accumulation triggers an inflammatory response, leading to the recruitment of immune cells and the production of pro-inflammatory cytokines, perpetuating plaque formation and instability.

PRRs, such as Toll-Like Receptors (TLRs) and scavenger receptors, recognize Pathogen-associated Molecular Patterns (PAMPs) and Damage- Associated Molecular Patterns (DAMPs) released during tissue injury. Activation of PRRs in arterial cells and immune cells triggers inflammatory signaling cascades, exacerbating atherosclerosis and promoting plaque rupture. Genetic variations in PRRs influence susceptibility to CVDs in animals, highlighting the importance of innate immune pathways in disease pathogenesis [2].

Description

Neutrophils are key effector cells of innate immunity involved in acute inflammation and tissue repair. In CVDs, neutrophils contribute to endothelial dysfunction, plaque destabilization and thrombosis through the release of reactive oxygen species and proteases. Monocytes differentiate into macrophages within atherosclerotic plaques, where they engulf lipid debris and secrete pro-inflammatory mediators, perpetuating vascular inflammation [3].

The complement system, a crucial component of innate immunity, contributes to CVD pathogenesis through various mechanisms. Dysregulation of complement activation promotes endothelial dysfunction, smooth muscle cell proliferation and plaque progression. Therapeutic targeting of complement components shows promise in mitigating CVD progression in animal models, underscoring the therapeutic potential of modulating innate immune pathways. Genetic predisposition influences susceptibility to CVDs in animals, with certain breeds exhibiting increased risk due to inherited traits affecting immune function and lipid metabolism. Environmental factors, such as diet, stress and exposure to pollutants, modulate innate immune responses and contribute to CVD development in animals [4].

Targeting innate immune pathways holds promise for the prevention and treatment of CVDs in animals. Immunomodulatory agents, including antiinflammatory drugs and monoclonal antibodies targeting specific immune mediators, show potential in reducing plaque inflammation and stabilizing atherosclerotic lesions. Nutritional interventions and lifestyle modifications that modulate innate immune function may complement conventional therapies for managing CVDs in animals [5].

Conclusion

Understanding the intricate interplay between innate immunity and cardiovascular diseases in animals provides insights into disease pathogenesis and therapeutic targets. Harnessing the immunomodulatory potential of innate immune pathways offers promising avenues for the prevention and treatment of CVDs in veterinary medicine. Further research is warranted to elucidate the specific mechanisms underlying innate immune dysregulation in different animal species and translate these findings into clinical practice for improved cardiovascular health in animals.

Acknowledgement

None.

Conflict of Interest

None.

References

1. Horton, Roger, Laurens Wilming, Vikki Rand and Ruth C. Lovering, et al. “Gene map of the extended human MHC.”Nat Rev Genet5 (2004): 889-899.

   Google Scholar, Crossref, Indexed at

2. Strawbridge, Andrew B. and Janice S. Blum. “Autophagy in MHC class II antigen processing.”Curr Opinion Immunol19 (2007): 87-92.

   Google Scholar, Crossref, Indexed at

3. Embgenbroich, Maria and Sven Burgdorf. “Current concepts of antigen cross-presentation.”Front Immunol9 (2018): 399581.

   Google Scholar, Crossref, Indexed at

4. Lees, Jason R. “CD8+ T cells: The past and future of immune regulation.”Cell Immunol357 (2020): 104212.

   Google Scholar, Crossref, Indexed at

5. Korn, Thomas, Mohamed Oukka, Vijay Kuchroo and Estelle Bettelli. “Th17 cells: Effector T cells with inflammatory properties.” Semni Immunol 19 (2007): 362-371.

   Google Scholar, Crossref, Indexed at